About

Corinne Engelman is a Vice Chair and Professor of Population Health Sciences at the University of Wisconsin–Madison, where she also serves as the Director of Graduate Programs. She earned her Master of Public Health in 2002 and her PhD in Epidemiology in 2006 from the University of Colorado Health Sciences Center. She has been a faculty member at UW–Madison since 2007. Her research focuses on the study design and data analysis of genetic, demographic, socioeconomic, behavioral, physiological, and environmental factors of complex diseases, with a particular emphasis on biomarkers and preclinical traits related to Alzheimer’s disease. Dr. Engelman’s group employs epidemiological, statistical, and bioinformatic approaches to analyze large-scale ‘omic data, including data from whole genome array genotyping, whole-genome sequencing, and mass spectrometry-based metabolomic, lipidomic, and proteomic analyses. Her work integrates ‘omic and questionnaire data to understand, predict, prevent, and treat health conditions. She is especially interested in identifying interactions with modifiable factors such as social, behavioral, and environmental influences to inform precision medicine and health. Dr. Engelman teaches courses in epidemiology and genetic epidemiology and is affiliated with several professional societies, including the American Society of Human Genetics, the International Genetic Epidemiology Society, and the International Society to Advance Alzheimer Research and Treatment.

Research topics

• Medicine
• Pathology
• Internal medicine
• Computer Science
• Neuroscience
• Biology
• Genetics
• Oncology
• Environmental health
• Computational biology
• Endocrinology
• Bioinformatics
• Data science
• Gerontology
• Psychiatry

Selected publications

• The Survey of the Health of Wisconsin (SHOW) Program: An Infrastructure for Advancing Population Health

  Frontiers in Public Health · 2022 · 52 citations

  • Computer Science
  • Environmental health
  • Data science

  Introduction: The Survey of the Health of Wisconsin (SHOW) was established in 2008 by the University of Wisconsin (UW) School of Medicine and Public Health (SMPH) with the goals of (1) providing a timely and accurate picture of the health of the state residents; and (2) serving as an agile resource infrastructure for ancillary studies. Today, the SHOW program continues to serve as a unique and vital population health research infrastructure for advancing public health. Methods: SHOW currently includes 5,846 adult and 980 minor participants recruited between 2008 and 2019 in four primary waves. WAVE I (2008-2013) includes annual statewide representative samples of 3,380 adults ages 21 to 74 years. WAVE II (2014-2016) is a triannual statewide sample of 1,957 adults (age ≥18 years) and 645 children (age 0-17). WAVE III (2017) consists of follow-up of 725 adults from the WAVE I and baseline surveys of 222 children in selected households. WAVEs II and III include stool samples collected as part of an ancillary study in a subset of 784 individuals. WAVE IV consists of 517 adults and 113 children recruited from traditionally under-represented populations in biomedical research including African Americans and Hispanics in Milwaukee, Wisconsin. Findings to Date: The SHOW resource provides unique spatially granular and timely data to examine the intersectionality of multiple social determinants and population health. SHOW includes a large biorepository and extensive health data collected in a geographically diverse urban and rural population. Over 60 studies have been published covering a broad range of topics including, urban and rural disparities in cardio-metabolic disease and cancer, objective physical activity, sleep, green-space and mental health, transcriptomics, the gut microbiome, antibiotic resistance, air pollution, concentrated animal feeding operations and heavy metal exposures. Discussion: The SHOW cohort and resource is available for continued follow-up and ancillary studies including longitudinal public health monitoring, translational biomedical research, environmental health, aging, microbiome and COVID-19 research.

  PublisherOA PDFDOI

• Cerebrospinal fluid metabolomics identifies 19 brain-related phenotype associations

  Communications Biology · 2021 · 167 citations

  • Biology
  • Computational biology
  • Genetics

  The study of metabolomics and disease has enabled the discovery of new risk factors, diagnostic markers, and drug targets. For neurological and psychiatric phenotypes, the cerebrospinal fluid (CSF) is of particular importance. However, the CSF metabolome is difficult to study on a large scale due to the relative complexity of the procedure needed to collect the fluid. Here, we present a metabolome-wide association study (MWAS), which uses genetic and metabolomic data to impute metabolites into large samples with genome-wide association summary statistics. We conduct a metabolome-wide, genome-wide association analysis with 338 CSF metabolites, identifying 16 genotype-metabolite associations (metabolite quantitative trait loci, or mQTLs). We then build prediction models for all available CSF metabolites and test for associations with 27 neurological and psychiatric phenotypes, identifying 19 significant CSF metabolite-phenotype associations. Our results demonstrate the feasibility of MWAS to study omic data in scarce sample types.

  DOI

• Genetic variants and functional pathways associated with resilience to Alzheimer’s disease

  Brain · 2020 · 141 citations

  • Neuroscience
  • Biology
  • Genetics

  Approximately 30% of older adults exhibit the neuropathological features of Alzheimer's disease without signs of cognitive impairment. Yet, little is known about the genetic factors that allow these potentially resilient individuals to remain cognitively unimpaired in the face of substantial neuropathology. We performed a large, genome-wide association study (GWAS) of two previously validated metrics of cognitive resilience quantified using a latent variable modelling approach and representing better-than-predicted cognitive performance for a given level of neuropathology. Data were harmonized across 5108 participants from a clinical trial of Alzheimer's disease and three longitudinal cohort studies of cognitive ageing. All analyses were run across all participants and repeated restricting the sample to individuals with unimpaired cognition to identify variants at the earliest stages of disease. As expected, all resilience metrics were genetically correlated with cognitive performance and education attainment traits (P-values < 2.5 × 10-20), and we observed novel correlations with neuropsychiatric conditions (P-values < 7.9 × 10-4). Notably, neither resilience metric was genetically correlated with clinical Alzheimer's disease (P-values > 0.42) nor associated with APOE (P-values > 0.13). In single variant analyses, we observed a genome-wide significant locus among participants with unimpaired cognition on chromosome 18 upstream of ATP8B1 (index single nucleotide polymorphism rs2571244, minor allele frequency = 0.08, P = 2.3 × 10-8). The top variant at this locus (rs2571244) was significantly associated with methylation in prefrontal cortex tissue at multiple CpG sites, including one just upstream of ATPB81 (cg19596477; P = 2 × 10-13). Overall, this comprehensive genetic analysis of resilience implicates a putative role of vascular risk, metabolism, and mental health in protection from the cognitive consequences of neuropathology, while also providing evidence for a novel resilience gene along the bile acid metabolism pathway. Furthermore, the genetic architecture of resilience appears to be distinct from that of clinical Alzheimer's disease, suggesting that a shift in focus to molecular contributors to resilience may identify novel pathways for therapeutic targets.

  DOI

• Association Between Common Variants in <i>RBFOX1</i>, an RNA-Binding Protein, and Brain Amyloidosis in Early and Preclinical Alzheimer Disease

  JAMA Neurology · 2020 · 97 citations

  • Medicine
  • Oncology
  • Internal medicine

  Importance: Genetic studies of Alzheimer disease have focused on the clinical or pathologic diagnosis as the primary outcome, but little is known about the genetic basis of the preclinical phase of the disease. Objective: To examine the underlying genetic basis for brain amyloidosis in the preclinical phase of Alzheimer disease. Design, Setting, and Participants: In the first stage of this genetic association study, a meta-analysis was conducted using genetic and imaging data acquired from 6 multicenter cohort studies of healthy older individuals between 1994 and 2019: the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study, the Berkeley Aging Cohort Study, the Wisconsin Registry for Alzheimer's Prevention, the Biomarkers of Cognitive Decline Among Normal Individuals cohort, the Baltimore Longitudinal Study of Aging, and the Alzheimer Disease Neuroimaging Initiative, which included Alzheimer disease and mild cognitive impairment. The second stage was designed to validate genetic observations using pathologic and clinical data from the Religious Orders Study and Rush Memory and Aging Project. Participants older than 50 years with amyloid positron emission tomographic (PET) imaging data and DNA from the 6 cohorts were included. The largest cohort, the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study (n = 3154), was the PET screening cohort used for a secondary prevention trial designed to slow cognitive decline associated with brain amyloidosis. Six smaller, longitudinal cohort studies (n = 1160) provided additional amyloid PET imaging data with existing genetic data. The present study was conducted from March 29, 2019, to February 19, 2020. Main Outcomes and Measures: A genome-wide association study of PET imaging amyloid levels. Results: From the 4314 analyzed participants (age, 52-96 years; 2478 participants [57%] were women), a novel locus for amyloidosis was noted within RBFOX1 (β = 0.61, P = 3 × 10-9) in addition to APOE. The RBFOX1 protein localized around plaques, and reduced expression of RBFOX1 was correlated with higher amyloid-β burden (β = -0.008, P = .002) and worse cognition (β = 0.007, P = .006) during life in the Religious Orders Study and Rush Memory and Aging Project cohort. Conclusions and Relevance: RBFOX1 encodes a neuronal RNA-binding protein known to be expressed in neuronal tissues and may play a role in neuronal development. The findings of this study suggest that RBFOX1 is a novel locus that may be involved in the pathogenesis of Alzheimer disease.

  DOI

Recent grants

• Genotype-gUIded vitamin D supplEmentation (GUIDE)

  NIH · $377k · 2015–2017

• Genomic and Metabolomic Data Integration in a Longitudinal Cohort at Risk for Alzheimer's Disease

  NIH · $3.8M · 2016–2027

• Genomic and Metabolomic Data Integration in a Longitudinal Cohort at Risk for Alzheimer's Disease

  NIH · $3.6M · 2016–2022

Frequent coauthors

• Sterling C. Johnson

  Temple University

  435 shared

• Sanjay Asthana

  Geriatric Research Education and Clinical Center

  294 shared

• Cynthia M. Carlsson

  University of Wisconsin–Madison

  290 shared

• Henrik Zetterberg

  UK Dementia Research Institute

  274 shared

• Kaj Blennow

  University of Gothenburg

  206 shared

• Ozioma C. Okonkwo

  Geriatric Research Education and Clinical Center

  196 shared

• Barbara B. Bendlin

  University of Wisconsin–Madison

  191 shared

• Burcu F. Darst

  178 shared

Labs

• The Engelman LabPI

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